Mutations in the spoIIIE gene of B. subtilis were first identified by their effects on sporulation, which they completely abolish (1). Although earlier work had suggested that SpoIIIE was involved in the regulation of gene expression during sporulation (2), we recently found that the primary defect in spoIIIE mutant cells lay in their failure to partition the prespore chromosome into the small, polar prespore compartment (3). In the mutant, only a small portion of the prespore chromosome (approximately 30%) enters the prespore; the remainder being left in the mother cell. The effects of the classical spoIIIE36 mutation on gene expression during sporulation could be explained by supposing that the mutation prevents genes from entering the prespore compartment. The model for SpoIIIE action presented by Wu et al (3) also explains the curious chromosome position effect that had previously been described for the effects of the spoIIIE36 mutation on gene expression (4). It seems that the small segment of DNA that enters the prespore compartment in the mutant is a specific one, so genes placed in this region are expressed normally. The same reporter gene, placed elsewhere in the chromosome is completely inactive, because the gene fails to gain access to the prespore.
As far as we know, no other mutations give rise to a spoIIIE-like phenotype. Functional studies of the protein suggest that it acts by forming a pore-like channel in the nascent spore septum, through which the prespore chromosome is driven in by a conjugation like mechanism (5). Although spoIIIE mutations have no obvious effect on vegetative growth, recent work in this laboratory has revealed that the protein can operate in vegetative cells if the normal machinery of chromosome segregation fails (6). This machinery works, in an as yet ill-defined manner, to separate the products of a round of DNA replication before the septum forms. However, if replication is delayed, e.g. by the action of an inhibitor such as nalidixic acid, the septum can close around the incompletely replicated nucleoid. In the presence of a functional spoIIIE gene, such cells can recover from this state, and the sister nucleoids eventually come to lie either side of the division septum. spoIIIE mutant cells with nucleoids trapped by septa can not recover and the nucleoid seems to be permanently trapped (6). In B. subtilis the spoIIIE defect is manifested in a reduction of about 2-fold in the resistance to drugs such as nalidixic acid and mitomycin C (6).
The finding of a vegetative role for SpoIIIE probably explains why the gene appears to be exceedingly well conserved in diverse members of the eubacteria (e.g. Coxiella burnetii, (7) and Campylobacter jejuni, (8)). Although its role is normally subsidiary to the primary partitioning machinery in vegetative B. subtilis, it may be that it has a more important role in other bacteria. In particular, we might predict a more important role for this function in bacteria in which the nascent nucleoids are more likely to be trapped by septa in normal conditions, such as in cocci and shorter rods. At least one preliminary report on Enterococcus appears to support this idea.